Sabrina de Souza Ferreira, Christopher Andrew Tibbitt
{"title":"Revisiting CD8<sup>+</sup> T Cells in Allergy: The Emerging Role of Tc2 Cells.","authors":"Sabrina de Souza Ferreira, Christopher Andrew Tibbitt","doi":"10.1111/sji.70146","DOIUrl":"10.1111/sji.70146","url":null,"abstract":"<p><p>Type 2 CD8<sup>+</sup> T (Tc2) cells are increasingly recognised as contributors to allergic inflammation, yet remain less well understood than T helper 2 (Th2) cells and Group 2 innate lymphoid cells (ILC2s). Defined by production of IL-4, IL-5 and IL-13, Tc2 cells have been implicated in eosinophilic inflammation, airway hyperresponsiveness, mucus production, and chronic tissue inflammation in diseases including asthma, atopic dermatitis, and chronic rhinosinusitis. Emerging evidence suggests that Tc2 differentiation and function are shaped by alarmins, lipid mediators, hypoxia, and immunometabolic pathways involving glycolysis, fatty acid metabolism, and serotonin signalling. Compared with Th2 cells, Tc2 cells may exhibit distinct features including tissue adaptation, responsiveness to innate inflammatory cues, and relative corticosteroid resistance, suggesting non-redundant roles in sustaining chronic allergic inflammation. Current biologic therapies targeting Type 2 pathways likely influence Tc2 activity, although their effects on Tc2-driven inflammation remain unclear. Here, we review current understanding of Tc2 cell phenotype, differentiation, immunometabolic regulation, and effector functions, and summarise evidence linking Tc2 cells to allergic disease. We also highlight key unanswered questions regarding Tc2 lineage stability, tissue residency, antigen specificity, and therapeutic targeting. Together, these findings position Tc2 cells as emerging amplifiers of Type 2 immunity and potential contributors to treatment-resistant allergic disease.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"104 3","pages":"e70146"},"PeriodicalIF":2.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13507951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148819426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The Role of Single-Nucleotide Polymorphisms in Acquired Aplastic Anaemia.","authors":"Yunxiao Luo, Teng Wang, Chen Han, Weilin Liu, Maoyuan Wang, Chunyi Lyu, Ruirong Xu","doi":"10.1111/sji.70149","DOIUrl":"10.1111/sji.70149","url":null,"abstract":"<p><p>Acquired aplastic anaemia (AA) is a heterogeneous disease characterized by bone marrow haematopoietic failure, and its pathogenesis is multifactorial, involving immune dysregulation, genetic susceptibility and environmental factors. Single-nucleotide polymorphisms (SNPs) are common single-base genomic variants that are frequent, stable and readily detectable, making them useful markers for studying genetic susceptibility to disease. Specific SNPs may contribute to immune abnormalities, bone marrow microenvironmental imbalance and dysfunction of haematopoietic stem and progenitor cells (HSPCs) in AA by regulating gene expression and influencing molecular functions. In this review, we systematically summarize the association between SNPs in key genes and the susceptibility, severity, treatment response and prognosis of AA, aiming to provide new insights into early risk prediction, disease management and potential gene-based intervention strategies for AA.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"104 3","pages":"e70149"},"PeriodicalIF":2.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13527175/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148865100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A Abrego-Peredo, C A Gallardo-Hernández, G López-Herrera, H Romero-Ramírez, F García-García, B Pineda-Olvera, J C Rodríguez-Alba
{"title":"Impact of CD38 Deficiency on B Cell Development in CD19-Deficient Mice.","authors":"A Abrego-Peredo, C A Gallardo-Hernández, G López-Herrera, H Romero-Ramírez, F García-García, B Pineda-Olvera, J C Rodríguez-Alba","doi":"10.1111/sji.70137","DOIUrl":"10.1111/sji.70137","url":null,"abstract":"<p><p>Physical interaction between the CD38 and CD19 proteins has been previously described. However, this association through the development of B lymphocytes has yet to be thoroughly investigated. To address this, we generated mice with a simultaneous absence of CD38 and CD19 proteins. Our results showed that Cd38 -/- Cd19 -/- mice had reduced survival. We suggest that the combined loss of CD38 and CD19 proteins results in normal B-cell maturation in the BM compared to WT mice. Nonetheless, these observations differ from those observed in Cd19 -/- mice. In DKO mice, a change in the proportion of the mature B-cell subset in BM was found in contrast to Cd38 -/- mice. On the periphery, reduced numbers of total splenocytes and total B cells were observed in DKO mice. In addition, some defects in splenic B-cell development were observed. For example, fewer absolute numbers of T1, T2, and mature B cells were found in comparison with WT mice. However, these subsets have no significant difference compared to Cd19 -/- mice. The MZ B-cell subset was almost depleted in Cd38-/-Cd19-/- mice, and a contrary effect was observed in FO B cells. Although not many differences were found in the proportions and absolute numbers during the different maturation stages of B cells between DKO and Cd19 -/- mice, a downward trend was observed in some of the steps during B-cell ontogeny. For this reason, the activation, proliferation, and immunoglobulin secretion, as well as the GC formation and MZ microenvironment in response to different stimuli, must be explored.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"104 2","pages":"e70137"},"PeriodicalIF":2.4,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13416008/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148607139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"From Validation to Clinical Interpretation: A Flow Cytometric Th17-Cell Assay for STAT1- and STAT3-Related Inborn Errors of Immunity.","authors":"Marie Juhl Toft, Camilla Darum Sørensen, Mette Christiansen, Carsten Schade Larsen, Mette Holm, Dinna Nedergaard, Rita Hansen, Lone Højbjerg Egedal, Nicklas Heine Staunstrup, Bjarne Kuno Møller, Mikkel Steen Petersen, Jens Magnus Bernth Jensen","doi":"10.1111/sji.70140","DOIUrl":"https://doi.org/10.1111/sji.70140","url":null,"abstract":"<p><p>Th17-cells are crucial for defence against fungal and bacterial infections and deficiency characterises certain inborn errors of immunity (IEI), including STAT3-related Hyper IgE syndrome (HIES) and STAT1-related Chronic Mucocutaneous Candidiasis (CMC). Standardised methods for clinical Th17-cell quantification are limited. We developed a flow cytometric assay for quantifying Th17-cells in peripheral blood based on PMA/ionomycin stimulation and intracellular IL-17 labeling and evaluated its precision, robustness and longitudinal stability. A reference interval was established in 51 healthy adults and the impact of age and sex was assessed. The assay was applied to 31 patients carrying STAT1 or STAT3 variants or presenting phenotypes for which Th17-cell quantification is informative. Diagnostic performance was analysed using receiver operating characteristic (ROC) curves and Matthew's Correlation Coefficients (MCC). The assay showed high intra- and inter-assay precision (CV 5.1% and 10%) and Th17-cell fractions remained stable after 72 h of post-fixation storage. Delayed pre-fixation reduced precision. Age and sex did not significantly influence Th17-cell fractions, supporting a unified Th17-cell reference interval of T-helper cells [0.21%-1.7%]. Compared with healthy controls, Th17-cell fractions were significantly lower in patients with STAT3 variants, patients with HIES or with both. ROC and MCC analyses indicated that Th17-cell fractions above 0.44% reliably excluded pathogenic variants or associated phenotypes in all patient groups. This validated Th17-cell assay is robust, reproducible and suitable for clinical use. It can guide genetic testing in IEI by identifying patients with Th17-cell deficiencies and excluding variants or phenotypes unlikely to be causative.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"104 2","pages":"e70140"},"PeriodicalIF":2.4,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13473723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148761919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Evolution and Mechanistic Insights of Immunometabolism in Metabolic Diseases and Infections.","authors":"Wenbin Tan","doi":"10.1111/sji.70141","DOIUrl":"10.1111/sji.70141","url":null,"abstract":"<p><p>Immunometabolism, an emerging field exploring metabolic reprogramming and functional regulation in immune cells, offers a lens for understanding complex diseases. This review delineates core concepts, key signalling nodes-emphasising the mechanistic target of rapamycin (mTOR) as an integrator of metabolic and immune signals-research and intervention strategies across metabolic and infectious diseases. Immune cells display metabolic plasticity: At rest, they depend mainly on mitochondrial oxidative phosphorylation, but swiftly shift to aerobic glycolysis upon activation to fuel effector functions. Pro-inflammatory subsets like Th1 cells and M1 macrophages lean heavily on glycolysis, whereas regulatory T cells favour fatty acid oxidation. Central pathways-glycolysis, the tricarboxylic acid (TCA) cycle, and amino acid metabolism-directly shape immune activation and inflammation via intermediates and regulatory enzymes. For example, succinate and itaconic acid are critical in inflammation control, while fatty acid and cholesterol metabolism dictate immune cell fate. In metabolic disorders such as obesity, diabetes, fatty liver disease, and atherosclerosis, immune metabolic reprogramming is the main driver of chronic low-grade inflammation and tissue injury. During infection, a metabolic tug-of-war ensues: Pathogens hijack host metabolism for survival, and the host counters by reprogramming its own metabolism. The idea of \"trained immunity\" highlights how metabolism-epigenetics crosstalk endows innate immunity with memory-like capacity. These insights inform therapeutic avenues-modulating metabolic pathways, nutritional interventions, and microbiome targeting-with wide potential. Challenges remain, including the complexity of in vivo networks and the need for precise interventions. Yet advances in single-cell multi-omics and metabolic flux analysis will deepen mechanistic understanding and enable breakthroughs in precision strategies.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"104 2","pages":"e70141"},"PeriodicalIF":2.4,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13478702/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148761882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The EBNA-1 Conundrum: Does Epstein-Barr Virus Invoke Autoimmune Pathology in a Population Subset by Poorly Purine-Loading Its Major Latency-Maintaining Transcript?","authors":"Donald R Forsdyke","doi":"10.1111/sji.70135","DOIUrl":"10.1111/sji.70135","url":null,"abstract":"<p><p>Viruses activate host defences by alerting interferon and other alarms. Viruses seeking latency must curtail this. Infected subjects would then have minimal immune system activation and remain healthy. However, a minority cannot prevent emergence of associated diseases. This conundrum remains despite our understanding (i) that interferon specifically suppresses the translation of viral mRNAs, but not host mRNAs, and (ii) that for the latent state only one latency-maintaining mRNA may be needed. Critical are mRNA loadings with purine (R) bases, relative to pyrimidine bases (Y). Base composition and structural studies have established the genome-wide potential of duplex DNA (hence transcripts thereof) to extruded stem-loops, the stems of which require parity between R and Y bases. Sometimes conflicting with coding demands, parity-violations (R > Y) decrease this potential in exons (and hence in mRNAs). Thus, one mRNA (EBNA-1) of the Epstein-Barr virus (EBV) is successful in not alerting hosts to immune awareness. However, Y-rich transcripts might occasionally arise in the highly polymorphic 'junk DNA', long known as pervasively transcribed. Thus, within a minor subset of the infected population, some may, by chance, have randomly mutated to create pyrimidine-loaded regions that would form forbidden double-stranded RNA duplexes with purine-loaded EBNA-1 mRNAs. Thus, immune systems would awaken. Other viruses, differing in types/extents of latency, have evolved different survival strategies. Thus, mRNAs of the extremely latent human T cell leukaemia virus (HTLV1) are Y-loaded (Y > R), but a single latency transcript is highly R-loaded. In contrast, most mRNAs of less extremely latent retrovirus (HIV1) are expressed with R > Y.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"104 1","pages":"e70135"},"PeriodicalIF":2.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13311203/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148346184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pedro Henrique Gallo-Francisco, Genesy Pérez Jorge, Guilherme Augusto Sanches Roque, Marina Flóro E Silva, Natália Scanavachia da Silva, Cecília Costa Fagundes, Alexandre Leite Rodrigues Oliveira, Fausto Almeida, Marcelo Brocchi, Selma Giorgio
{"title":"Impact of Bacterial Membrane Vesicles on Cellular Responses in Leishmania amazonensis-Infected Macrophages In Vitro.","authors":"Pedro Henrique Gallo-Francisco, Genesy Pérez Jorge, Guilherme Augusto Sanches Roque, Marina Flóro E Silva, Natália Scanavachia da Silva, Cecília Costa Fagundes, Alexandre Leite Rodrigues Oliveira, Fausto Almeida, Marcelo Brocchi, Selma Giorgio","doi":"10.1111/sji.70136","DOIUrl":"10.1111/sji.70136","url":null,"abstract":"<p><p>Leishmania amazonensis is an intracellular protozoan parasite and etiological agent of Localised Cutaneous Leishmaniasis (LCL). A challenge in managing LCL is the frequent occurrence of secondary bacterial co-infections caused by opportunistic bacteria such as Pseudomonas aeruginosa and Staphylococcus aureus. This study aimed to evaluate the effects of Bacterial Membrane Vesicles (BMVs) from these bacteria on macrophages infected with L. amazonensis. BMVs were characterised by Nanoparticle Tracking Analysis (NTA), and their effects on macrophage viability, infection dynamics, and cytokine production were assessed. Macrophages infected with L. amazonensis and subsequently treated with BMVs exhibited reduced parasite burden and cell viability compared to infected controls. The production of cytokines was variably modulated depending on the vesicle source. TNF-α levels were higher in macrophages infected with L. amazonensis and treated with BMVs than in those infected with the parasite alone. Additionally, elevated levels of IL-1β were observed in co-cultures treated with P. aeruginosa membrane vesicles (POMVs), suggesting a stronger inflammatory profile than that induced by S. aureus extracellular vesicles (SEVs). In contrast, IL-4 and IL-6 levels were not significantly affected by either POMVs or SEVs. These results indicate that uninfected and L. amazonensis-infected macrophages respond distinctly to POMVs and SEVs, particularly through enhanced secretion of IL-1β and TNF-α. In conclusion, macrophages exposed to both L. amazonensis and bacterial vesicles simulate a host-parasite-bacteria interaction, activating production of cytokines. Given their immunogenic properties, BMVs may represent promising targets for the development of therapeutic strategies associated with LCL.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"104 1","pages":"e70136"},"PeriodicalIF":2.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13354861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148423711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Joonatan Mattila, Nelli Heikkilä, Iivo Hetemäki, Joonatan Borchers, Outi Mäkitie, Saila Laakso, T Petteri Arstila
{"title":"Unsupervised Flow Cytometry Reveals a Constant Shift Towards Activated CD4<sup>+</sup> T Cell Subsets in APECED.","authors":"Joonatan Mattila, Nelli Heikkilä, Iivo Hetemäki, Joonatan Borchers, Outi Mäkitie, Saila Laakso, T Petteri Arstila","doi":"10.1111/sji.70134","DOIUrl":"10.1111/sji.70134","url":null,"abstract":"<p><p>Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is a rare monogenic autoimmune disease caused by loss-of-function mutations in the Autoimmune regulator gene and the subsequent impairment of negative selection in the thymus. Previous studies have identified many T cell abnormalities in APECED patients, with increased signs of activation and failure of regulation. These findings, however, have been demonstrated using traditional flow cytometry studies, prone to human misinterpretation of multidimensional data. Here we present an unsupervised flow cytometry analysis of CD4<sup>+</sup> T cells in 20 APECED patients. Our workflow consists of an optimized sequence of well documented unsupervised analysis algorithms for data quality control, batch correction and clustering with multiple options evaluated. We show the overall increase in T cell activation to extend from the previously reported CD8<sup>+</sup> compartment to both the T helper and regulatory T cells. We demonstrate the regulatory T cells in APECED to adopt a population distribution dominated by cells of low suppressive potential and present a novel CD45RA<sup>neg</sup>, CCR7<sup>neg</sup>, CD31<sup>high</sup>, CD127<sup>mid</sup> population unique to APECED. In general, however, we find the population structure of the APECED CD4<sup>+</sup> T cell compartment largely similar to that of the controls as supported by both our clustering and dimensionality reduction analyses. Our analysis replicates previous findings and provides novel information on APECED while also presenting an optimized unsupervised workflow for flow cytometry analysis in general. Our approach offers multiple advantages over manual flow cytometry analysis with its rigorous data quality control, well-documented batch correction and optimized automated clustering.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"104 1","pages":"e70134"},"PeriodicalIF":2.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13307629/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148339922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Recent Thymic Emigrant Levels in Inborn Errors of Immunity: Is Their Diagnostic Value Greater Than We Think?","authors":"Selami Ulaş, Serdar Al, Sezin Naiboğlu, Kübra Yırgın, Sibel Kaplan, Gülşah Kalay, Nermin Kapçı, Özge Türkyılmaz Uçar, Erkan Çakmak, Ahmet Sert, Meryem Özçelik, Burcu Çil, Şeyda Köse, Simge Kılıçoğlu, Pınar Gökmirza, Çiğdem Aydoğmuş","doi":"10.1111/sji.70133","DOIUrl":"https://doi.org/10.1111/sji.70133","url":null,"abstract":"<p><p>We aimed to evaluate the sensitivity and specificity of Recent Thymic Emigrant (RTE) levels for diagnostic discrimination among various Inborn Errors of Immunity (IEI) subgroups. We analysed 205 paediatric patients diagnosed with IEI at the Paediatric Immunology and Allergy Department of Başakşehir Çam and Sakura City Hospital in Istanbul between January 2021 and January 2024. An age- and sex-matched control group consisting of 31 healthy children was also included for comparison. Demographic, clinical and laboratory data were evaluated. Reduced RTE levels were identified in 39% of all patients. Low RTE levels were most pronounced in patients with syndromic combined immunodeficiency (77%) and immune dysregulation (100%), and were also observed at high frequencies in combined immunodeficiency (CID) (60%) and autoinflammatory disorders (57.1%). For the syndromic CID group, the diagnostic performance of RTE yielded an area under the curve (AUC) of 0.80, with a sensitivity of 92% and a specificity of 52%. In the immune dysregulation group, the AUC was 0.79, with a sensitivity of 83.5% and a specificity of 57.1%. Assessment of RTE levels represents a valuable diagnostic biomarker, particularly for patients within the syndromic CID and immune dysregulation categories. This parameter may contribute meaningfully to clinical practice by facilitating early diagnosis, guiding genetic testing and enabling assessment of thymic function. Incorporating thymic output assessment into routine immunophenotyping panels may shorten the diagnostic timeline for IEI and allow earlier initiation of appropriate therapies.</p>","PeriodicalId":21493,"journal":{"name":"Scandinavian Journal of Immunology","volume":"104 1","pages":"e70133"},"PeriodicalIF":2.4,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148369644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}